Method of improving tolerance of plants to herbicides using seed insecticide treatments

Methods of increasing the tolerance of a plant to an herbicide and seeds for carrying out these methods are provided herein. The methods include treating the seeds of the plant with an insecticide prior to planting. The insecticide treatment makes the resulting plant more resistant to herbicides and in particular to post-emergence herbicides as compared to untreated seeds. The plants suitably do not have complete natural or complete engineered resistance to the herbicide. The treated seeds are then planted in a field and the herbicide is applied to the field. The resulting plants growing from the treated seeds have increased tolerance to the herbicide as compared to plants grown from seeds not treated with the insecticide

Herbicide-resistant Grain Sorghum

A fluazifop-resistant sorghum cultivar designated ‘21534_ACCase-R’ and plants comprising a polynucleotide encoding the polypeptide of SEQ ID NO: 39 are disclosed herein. The present invention provides seeds, plants, and plant parts derived from sorghum cultivar ‘21534_ACCase-R’ and those including SEQ ID NO: 39. Further, it provides methods for producing a sorghum plant by crossing ‘21534_ACCase-R’ with itself or another sorghum variety. The invention also encompasses any sorghum seeds, plants, and plant parts produced by the methods disclosed herein, including those in which additional traits have been transferred into ‘21534_ACCase-R’ through the introduction of a transgene or by breeding ‘21534_ACCase-R’ with another sorghum cultivar

Herbicide-resistant Grain Sorghum

A fluazifop-resistant sorghum cultivar designated ‘21534_ACCase-R’ and plants comprising a polynucleotide encoding the polypeptide of SEQ ID NO: 39 are disclosed herein. The present invention provides seeds, plants, and plant parts derived from sorghum cultivar ‘21534_ACCase-R’ and those including SEQ ID NO: 39. Further, it provides methods for producing a sorghum plant by crossing ‘21534_ACCase-R’ with itself or another sorghum variety. The invention also encompasses any sorghum seeds, plants, and plant parts produced by the methods disclosed herein, including those in which additional traits have been transferred into ‘21534_ACCase-R’ through the introduction of a transgene or by breeding ‘21534_ACCase-R’ with another sorghum cultivar

Confirmation of S-metolachlor resistance in Palmer amaranth (Amaranthus palmeri)

AbstractS-Metolachlor is commonly used by soybean and cotton growers, especially with POST treatments for overlapping residuals, to obtain season-long control of glyphosate- and acetolactate synthase (ALS)–resistant Palmer amaranth. In Crittenden County, AR, reports of Palmer amaranth escapes following S-metolachlor treatment were first noted at field sites near Crawfordsville and Marion in 2016. Field and greenhouse experiments were conducted to confirm S-metolachlor resistance and to test for cross-resistance to other very-long-chain fatty acid (VLCFA)–inhibiting herbicides in Palmer amaranth accessions from Crawfordsville and Marion. Palmer amaranth control in the field (soil <3% organic matter) 14 d after treatment (DAT) was ≥94% with a 1× rate of acetochlor (1,472 g ai ha–1; emulsifiable concentrate formulation) and dimethenamid-P (631 g ai ha–1). However, S-metolachlor at 1,064 g ai ha–1 provided only 76% control, which was not significantly different from the 1/2× and 1/4× rates of dimethenamid-P and acetochlor (66% to 85%). In the greenhouse, Palmer amaranth accessions from Marion and Crawfordsville were 9.8 and 8.3 times more resistant to S-metolachlor compared with two susceptible accessions based on LD50 values obtained from dose–response experiments. Two-thirds and 1.5 times S-metolachlor at 1,064 g ha–1 were the estimated rates required to obtain 90% mortality of the Crawfordsville and Marion accessions, respectively. Data collected from the field and greenhouse confirm that these accessions have evolved a low level of resistance to S-metolachlor. In an agar-based assay, the level of resistance in the Marion accession was significantly reduced in the presence of a glutathione S-transferase (GST) inhibitor, suggesting that GSTs are the probable resistance mechanism. With respect to other VLCFA-inhibiting herbicides, Marion and Crawfordsville accessions were not cross-resistant to acetochlor, dimethenamid-P, or pyroxasulfone. However, both accessions, based on LD50 values obtained from greenhouse dose–response experiments, exhibited reduced sensitivity (1.5- to 3.6-fold) to the tested VLCFA-inhibiting herbicides

Resistance of Echinochloa crus-galli

Three Echinochloa crus-galli (barnyardgrass) populations from rice fields in Arkansas (AR1 and AR2) and Mississippi (MS1), USA, were recently confirmed to be resistant to imazethapyr. Experiments were conducted to characterize cross-resistance to acetolactate synthase- (ALS-) inhibiting herbicides and determine if malathion, a known cytochrome P450 monooxygenase (CYP) inhibitor, would overcome resistance. The AR1 and MS1 populations were cross-resistant to bispyribac-sodium; however, AR2 was sensitive to bispyribac-sodium. The AR1, AR2, and MS1 populations were >94, >94, and 3.3 times, respectively, more resistant to imazamox; >94, 30, and 9.4 times, respectively, more resistant to penoxsulam; and 15, 0.9, and 7.2 times, respectively, more resistant to bispyribac-sodium compared to a susceptible population. Addition of malathion to penoxsulam reduced dry weight of all populations and increased mortality of AR2 and MS1 populations compared to penoxsulam alone. Addition of malathion to imazethapyr and bispyribac-sodium increased the mortality of MS1 population in mixture with imazethapyr and AR1 population in mixture with bispyribac-sodium compared to treatments with imazethapyr and bispyribac-sodium applied alone. Synergism of ALS-inhibiting herbicides with malathion indicates increased herbicide degradation by CYP as partial mechanism of resistance to penoxsulam in all resistant populations and probably to imazethapyr in MS1 and bispyribac-sodium in AR1 populations

Herbicide-resistant weeds : from research and knowledge to future needs

Synthetic herbicides have been used globally to control weeds in major field crops. This has imposed a strong selection for any trait that enables plant populations to survive and reproduce in the presence of the herbicide. Herbicide resistance in weeds must be minimized because it is a major limiting factor to food security in global agriculture. This represents a huge challenge that will require great research efforts to develop control strategies as alternatives to the dominant and almost exclusive practice of weed control by herbicides. Weed scientists, plant ecologists and evolutionary biologists should join forces and work towards an improved and more integrated understanding of resistance across all scales. This approach will likely facilitate the design of innovative solutions to the global herbicide resistance challenge

4-Hydroxyphenylpyruvate Dioxygenase (HPPD)-Inhibiting Herbicides: Past, Present, and Future

The 4-hydroxyphenylpyruvate dioxygenase (HPPD)-inhibiting herbicides are primarily used for weed control in corn, barley, oat, rice, sorghum, sugarcane, and wheat production fields in the United States. The objectives of this review were to summarize (1) the history of HPPD-inhibitor and their use in the United States, (2) HPPD-inhibitor resistant weeds, their mechanism of resistance, and management, (3) interaction of HPPD-inhibitor with other herbicides, and (4) the future of HPPD-inhibitor-resistant crops. As of 2022, three broadleaf weeds (Palmer amaranth, waterhemp, and wild radish) have evolved resistance to the HPPD-inhibitor. The predominance of metabolic resistance to HPPD-inhibitor was found in aforementioned three weed species. Management of HPPD-inhibitor-resistant weeds can be accomplished using alternate herbicides such as glyphosate, glufosinate, 2,4-D, or dicamba; however, metabolic resistance poses a serious challenge, as the weeds may be cross-resistant to other herbicide sites of action, leading to limited herbicide options. The HPPD-inhibitor is commonly applied with photosystem II (PS II)-inhibitor to increase efficacy and weed control spectrum. The synergism with HPPD-inhibitor arises from depletion of plastoquinones, which allows increased binding of PS II-inhibitor to the D1 protein. New HPPD-inhibitor from azole carboxamides class is in development and expected to be available in the near future. The HPPD-inhibitor-resistant crops have been developed through overexpression of a resistant bacterial HPPD enzyme in plants and the overexpression of transgenes for HPPD and a microbial gene that enhances the production of HPPD substrate. Isoxaflutole-resistant soybean is commercially available, and it is expected that soybean resistant to other HPPD-inhibitor such as mesotrione, stacked with resistance to other herbicides, will be available in the near future

Seedbank Persistence of Palmer Amaranth (\u3ci\u3eAmaranthus palmeri\u3c/i\u3e) and Waterhemp (\u3ci\u3eAmaranthus tuberculatus\u3c/i\u3e) across Diverse Geographical Regions in the United States

Knowledge of the effects of burial depth and burial duration on seed viability and, consequently, seedbank persistence of Palmer amaranth (Amaranthus palmeri S. Watson) and waterhemp [Amaranthus tuberculatus (Moq.) J. D. Sauer] ecotypes can be used for the development of efficient weed management programs. This is of particular interest, given the great fecundity of both species and, consequently, their high seedbank replenishment potential. Seeds of both species collected from five different locations across the United States were investigated in seven states (sites) with different soil and climatic conditions. Seeds were placed at two depths (0 and 15cm) for 3 yr. Each year, seeds were retrieved, and seed damage (shrunken, malformed, or broken) plus losses (deteriorated and futile germination) and viability were evaluated. Greater seed damage plus loss averaged across seed origin, burial depth, and year was recorded for lots tested at Illinois (51.3% and 51.8%) followed by Tennessee (40.5% and 45.1%) and Missouri (39.2% and 42%) for A. palmeri and A. tuberculatus, respectively. The site differences for seed persistence were probably due to higher volumetric water content at these sites. Rates of seed demise were directly proportional to burial depth (α=0.001), whereas the percentage of viable seeds recovered after 36 mo on the soil surface ranged from 4.1% to 4.3% compared with 5% to 5.3% at the 15-cm depth for A. palmeri and A. tuberculatus, respectively. Seed viability loss was greater in the seeds placed on the soil surface compared with the buried seeds. The greatest influences on seed viability were burial conditions and time and site-specific soil conditions, more so than geographical location. Thus, management of these weed species should focus on reducing seed shattering, enhancing seed removal from the soil surface, or adjusting tillage systems